Since AIDS was first diagnosed, 30 years ago this week, HIV has infected more than 60 million people, half of whom have died. Only one person has been found to be cured of HIV, however — known as the “Berlin patient.” In this week’s New York magazine, Tina Rosenberg tells his story.

[Timothy] Brown is a 45-year-old translator of German who lives in San Francisco. He is of medium height and very skinny, with thinning brown hair. He found out he had HIV in 1995. He had not been tested for the virus in half a decade, but that year a former partner turned up positive. “You’ve probably got only two years to live,” the former partner told him when Brown got his results.

His partner was wrong — lifesaving antiretrovirals were about to arrive — and Brown spent the next ten years living in Berlin, pursuing his career and enjoying the city by night.

The antiretroviral drugs that saved Brown’s life have turned AIDS from a virtual death sentence into a chronic illness for the 5 million people worldwide who have access to them. But despite increasing evidence that early treatment with these drugs can reduce the odds of HIV transmission — by 96%, according to one study — more than 8,000 Americans are on waiting lists for treatment as states cut funding because of the recession.

In Brown’s case, however, the drugs are no longer necessary. A decade after finding out he had HIV, Brown was diagnosed with leukemia, yet another life-threatening disease. In the end, though, that diagnosis might be what saved his life. For treatment of his cancer, Brown happened to see an enterprising doctor who wondered, what if we could cure both the blood cancer and the AIDS with the same therapy?

Brown was referred to Charité Medical University, where he was treated by Gero Hütter, a 37-year-old ­specialist in blood cancers.

After chemo, the leukemia came back. Brown’s last chance was a stem-cell transplant from a bone-marrow donor. Hütter had an idea. He knew little about HIV, but he remembered that people with a certain natural genetic mutation are very resistant to the virus. The mutation, called delta 32, disables CCR5, a receptor on the surface of immune-system cells that, in the vast majority of cases, is HIV’s path inside. People with copies from both parents are almost completely protected from getting HIV, and they are relatively common in northern Europe — among Germans, the rate is about one in a hundred. Hütter resolved to see if he could use a stem-cell donor with the delta-32 ­mutation to cure not just Brown’s leukemia but also his HIV.

For more of Brown and Hütter’s story — and why AIDS researchers have long eschewed the search for a cure — see here. As the 30th anniversary of AIDS approaches and a vaccine remains elusive, Rosenberg suggests a cure may not be.